Exhaustion of the Frank–Starling mechanism in conscious dogs with heart failure induced by chronic coronary microembolization

“…The daily coronary microembolization results in a multifocal pattern of scarring and large scattered areas of fibrosis and granulomas surrounding large clusters of microbeads in the LV myocardium [4]. The reproducibility and stability of this CHF model have been demonstrated by our group and other investigators [4,[7][8][9][10].…”

Section: Coronary Embolization-induced Heart Failurementioning

confidence: 61%

“…A daily coronary-embolization (Embo) model, which has been well established for inducing stable but severe systolic and diastolic dysfunction [4,[7][8][9][10], was used in 10 mongrel dogs to create CHF. After a stable CHF was established by daily Embo, a thoracotomy was performed, and an LVSD was implanted in five treatment animals.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Effect of passive cardiac containment on ventricular synchrony and cardiac function in awake dogs

George

Cheng

et al. 2007

European Journal of Cardio-Thoracic Surgery

Self Cite

View full text Add to dashboard Cite

Objective: Passive restraint of the left ventricle (LV) has been shown to have beneficial effects on acute hemodynamics and reverse remodeling in both animal and human models. The goals of this study were to test whether a left ventricular support device (LVSD) improves LV synchrony and/ or affects cardiac performance. Methods: Ten dogs were chronically instrumented to measure hemodynamics and LV volume (sonomicrometry). Congestive heart failure (CHF) was induced by repeated intracoronary microembolization via a chronically implanted coronary catheter. The LVSD was implanted after establishment of CHF in five animals, and five animals were observed as controls. All animals were then observed for 8 weeks.A mathematical model to measure LV synchrony was used to evaluate LV motion over time. Results: Mean arterial pressure and LV pressures was significantly increased after LVSD therapy, and LV pressure-volume relationships were shifted leftwards, although no change was seen in ejection fraction, end-systolic elastance, or LV dP/dt versus control. There was no significant change in diastolic function in LVSD animals compared with control animals. End-diastolic volumes were reduced by 15% after 8 weeks with LVSD treatment, versus an increase of 8% in control animals ( p < 0.05). Synchrony was significantly improved with LVSD therapy compared with control (9% vs 76% of baseline) in 1 of 11 ventricular dimension axes (Anterior-Apex). Conclusions: LVSD therapy provided only minimal improvement in ventricular synchrony and partially improved hemodynamics. Further study into mechanisms of benefit are warranted. #

show abstract

“…Clinical studies revealed that patients exhibiting no-reflow following reperfusion therapy for acute myocardial infarction (AMI) were associated with worse prognosis compared to patients without no-flow [1,2]. Currently, the mechanism of no-reflow has been exclusively studied in animal models of coronary artery ligation/ reperfusion [5] and coronary microembolization (CME) [3][4][5] in canine or pig models, as well as in the rat coronary autologous coronary thrombotic microembolism model [6]. However, ischemia/reperfusion model in pig and canine only partly reflects pathological changes of no-reflow, since clinical "no-reflow" phenomenon is largely induced by microemboli [1] but not induced by coronary artery occlusion.…”

mentioning

confidence: 99%

Establishment of an experimental angiographic slow coronary flow model by microsphere embolism in swines

Hu¹,

Bai²,

Gu³

et al. 2014

International Journal of Cardiology

View full text Add to dashboard Cite

No-reflow or slow-flow post revascularization remains a challenge in interventional cardiology. The "no-reflow" phenomenon is largely induced by microemboli of atherosclerotic debris, spasm, microvascular damage, and thrombi generated by percutaneous coronary intervention (PCI) procedure [1]. Clinical studies revealed that patients exhibiting no-reflow following reperfusion therapy for acute myocardial infarction (AMI) were associated with worse prognosis compared to patients without no-flow [1,2]. Currently, the mechanism of no-reflow has been exclusively studied in animal models of coronary artery ligation/ reperfusion [5] and coronary microembolization (CME) [3][4][5] in canine or pig models, as well as in the rat coronary autologous coronary thrombotic microembolism model [6]. However, ischemia/reperfusion model in pig and canine only partly reflects pathological changes of no-reflow, since clinical "no-reflow" phenomenon is largely induced by microemboli [1] but not induced by coronary artery occlusion. Recently, Ma et al. reported that continuous injection of 120,000 42 μm microspheres into the left anterior descending (LAD) did not induce changes on coronary thrombolysis in myocardial infarction (TIMI) grade and TIMI 3 coronary flow was maintained immediately after microembolization and hemodynamic parameters remained stable before and after CME [7]. Till now, there is no large animal model presenting angiographic evidence of slow flow.In this study, we established an angiographic coronary slow flow model in pig by repeated coronary injection of small doses of 40 μm microspheres. Eight male domestic pigs (3 to 4 months old, 25 ± 2 kg) were used in this study. Aspirin (2-3 mg/kg/d) was mixed in the food 3 days prior to experimental studies. All animals received humane care and that study protocols comply with the institution's guidelines.Pigs were anesthetized by an intramuscular injection of ketamine (15 mg/kg) combining with atropine (1 mg) and then fixed in a supine position on the workstation, 3-5 ml 3% pentobarbital sodium solution was injected via ear marginal vein on demand to maintain the anesthesia state. Oxygen saturation (SO 2 ) was measured with pulse oximeter. Anticoagulation was induced with 200 IU/kg heparin sodium. The right femoral artery was dissected and a 6 F vascular sheath was placed for arterial access. After initial coronary angiography (CAG) using 6 F JR3.5 guiding catheter (Medtronic, Inc.), ventriculography and LV pressure measurements with 5 F Pigtail catheter (Cordis Inc.), a 2.6 F infusion microtubule catheter (Terumo Corporation) was then placed at the middle part of the LAD artery for microsphere injection, and 0.1 ml stock solution with 12,000 microspheres was diluted in 5 ml saline and injected for 20 s through the 2.6 F infusion microtubule catheter; this procedure was repeated, followed by 2 × 0.2 ml stock solution diluted into 5 ml saline with 24,000 microsphere injection, then 0.3 ml stock solution diluted into 5 ml saline with 36,000 microsphere injection (interval bet...

show abstract

Exhaustion of the Frank–Starling mechanism in conscious dogs with heart failure induced by chronic coronary microembolization

Cited by 23 publications

References 23 publications

Repercussões cardíacas após infarto do miocárdio em ratas submetidas previamente a exercício físico

Repercussões cardíacas após infarto do miocárdio em ratas submetidas previamente a exercício físico

Effect of passive cardiac containment on ventricular synchrony and cardiac function in awake dogs

Establishment of an experimental angiographic slow coronary flow model by microsphere embolism in swines

Contact Info

Product

Resources

About